Department of Experimental Medical Science, Lund University, Lund, Sweden.
J Periodontal Res. 2010 Dec;45(6):796-802. doi: 10.1111/j.1600-0765.2010.01308.x.
Estrogen modulates inflammatory responses, but the mechanisms involved have not yet been identified. Periodontal ligament (PDL) cells produce chemokines (a group of chemoattractant molecules that recruit leukocytes) and it has been suggested that estrogen modulates periodontal inflammation by regulating the expression of chemokines by PDL cells. Therefore, the objectives of this study were to investigate the regulation of chemokine ligand 2 [CCL2/monocyte chemoattractant protein 1 (MCP-1)], chemokine ligand 3 [CCL3/macrophage inflammatory protein-1α (MIP-1α)] and chemokine ligand 5 (CCL5/RANTES) by estrogen in human PDL cells.
PDL cells were obtained from the PDL of premolars, extracted for orthodontic reasons, from two boys and two girls (16 and 17 years of age). PDL cell CCL2, CCL3 and CCL5 mRNA transcripts were determined by quantitative real-time PCR. The concentrations of CCL2, CCL3 and CCL5 proteins were determined by ELISAs.
Treatment with 0.5 μg/mL of lipopolysaccharide (LPS, from Escherichia coli) + 100 nm 17β-estradiol (E(2) ) for 24 h reduced the expression of CCL3 mRNA by about 40% compared to PDL cells treated with LPS alone. Attenuation of CCL3 mRNA was not associated with a decrease in CCL3 protein within 48 h, suggesting a slow turnover of the CCL3 protein. Interindividual differences in the effects of E(2) on CCL5 mRNA expression were observed. E(2) (100 nm) increased the expression of CCL5 by 40-60% in PDL cells derived from two subjects but reduced the expression of CCL5 by about 30% in cells from another subject. CCL2 mRNA and CCL2 protein were highly expressed, but not regulated by E(2) . Similar data were observed in cells obtained from both boys and girls.
Regulation, by estrogen, of chemokine expression in PDL cells shows a complex pattern involving the down-regulation as well as the up-regulation of chemokines, suggesting that estrogen exerts both anti-inflammatory and proinflammatory effects through these mechanisms.
雌激素可调节炎症反应，但其中的具体机制尚未明确。牙周韧带（PDL）细胞可产生趋化因子（一组趋化分子，可募集白细胞），有观点认为雌激素可通过调节 PDL 细胞趋化因子的表达来调节牙周炎症。因此，本研究旨在探讨雌激素对人牙周膜细胞中趋化因子配体 2 [CCL2/单核细胞趋化蛋白 1（MCP-1）]、趋化因子配体 3 [CCL3/巨噬细胞炎性蛋白 1α（MIP-1α）]和趋化因子配体 5（CCL5/RANTES）的调节作用。
从因正畸需要而拔除的 2 名 16 岁男孩和 2 名 17 岁女孩的前磨牙 PDL 中提取 PDL 细胞，采用实时定量 PCR 法检测 PDL 细胞 CCL2、CCL3 和 CCL5 mRNA 转录本，ELISA 法检测 CCL2、CCL3 和 CCL5 蛋白浓度。
与单独用脂多糖（LPS，来自大肠杆菌）处理的 PDL 细胞相比，用 0.5 μg/mL LPS+100nm 17β-雌二醇（E2）处理 24 h 可使 CCL3 mRNA 的表达降低约 40%。48 h 内 CCL3 蛋白未见减少，提示 CCL3 蛋白半衰期较长。E2 对 CCL5 mRNA 表达的影响存在个体间差异。E2（100nm）可使 2 名供体的 PDL 细胞中 CCL5 的表达增加 40%~60%，但使另 1 名供体的 PDL 细胞中 CCL5 的表达减少约 30%。CCL2 mRNA 和 CCL2 蛋白表达水平较高，但不受 E2 调节，在来自男孩和女孩的细胞中观察到相似的数据。
雌激素对 PDL 细胞中趋化因子表达的调节呈现复杂模式，包括趋化因子的下调和上调，提示雌激素通过这些机制发挥抗炎和促炎作用。
